**If you suspect your horse has laminitis or is ill, always consult your vet and discuss all aspects of management/treatment with him/her.**

]]>Wed, 16 Nov 2016 00:00:00 GMThttp://www.thelaminitissite.org/articles/pituitary-stress-hormones​Sometimes ACTH produced normally by the pars distalis (PD) as part of the hypothalamic-pituitary-adrenal (HPA) axis appears to be confused with ACTH produced by the pars intermedia (PI) due to lack of dopaminergic inhibition in horses with PPID.

All horses, whether they have PPID or not, react to a stress stimulus as follows:CRH and AVP (vasopressin) are released by paraventricular neurons in the hypothalamus.CRH and AVP stimulate corticotropes in the pars distalis (or anterior pituitary) of the pituitary gland to secrete ACTH.ACTH travels in the blood to the adrenal glands, on top of the kidneys, where it stimulates the adrenal glands to release cortisol.Cortisol is carried in the blood back to the hypothalamus and the pars distalis of the pituitary gland, which recognize the high levels of cortisol, and decrease or turn off CRH, AVP and ACTH release - this is called negative feedback, it prevents excessive hormone production.

In a normal horse, the pars intermedia produces a peptide called POMC, which is changed to ACTH by an enzyme, PC1, then nearly all the ACTH is changed into alpha-MSH, beta-endorphin, CLIP and other hormones by another enzyme, PC2. Hormone production in the PI is controlled by dopamine, released by hypothalamic periventricular dopaminergic neurons, interacting with D2 dopamine receptors on the ​PI.

In horses with PPID, dopamine producing neurons are lost, and with less dopamine to inhibit hormone production, the PI releases massively increased amounts of alpha-MSH, beta-endorphin and CLIP, and also ACTH.

In a normal horse, only around 2% of circulating ACTH is made in the pars intermedia, 98% comes from the pars distalis, and dopamine plays no part in controlling normal ACTH output from the PD.

The excess levels of alpha-MSH, beta-endorphin and CLIP are thought to contribute to causing the clinical signs of PPID. The plasma ACTH in PPID horses is thought to be less biologically active than plasma ACTH in normal horses, which may explain why horses with PPID rarely have above normal cortisol levels. The lack of dopamine and increase in POMC-derived hormones leads to an increase in the number (hyperplasia) and size (hypertrophy) of the cells in the PI, eventually leading to adenoma (tumour) formation - this has nothing to do with cortisol.

In her 2011 paper on Equine PPID, Dr McFarlane states that pituitary antioxidant capacity has not been shown to be impaired in horses with PPID, but that the impairment of the activity of pituitary manganese superoxide dismutase found in older horses may contribute to the risk of PPID developing with age.

She goes on to say that excellent nutrition is important for horses with PPID, and that in theory, feeds high in antioxidants could slow the neurodegenerative process associated with PPID, but that there is currently no evidence for this. Early treatment with pergolide to replace the missing dopamine and reduce excess hormone production and the clinical signs of PPID is advised. Interestingly, research by Gille et al. (2002) found that "pergolide protects dopaminergic neurons under conditions of elevated oxidative stress"; similarly research by Uberti et al. in the same year suggested that "pergolide ... may interfere with the early phases of the oxidative stress-induced neurotoxic process". Dr McFarlane theorises that any antioxidant and neuroprotective properties of pergolide could be beneficial in slowing the progression of PPID.

So in conclusion, optimal management and treatment with pergolide is recommended for horses with PPID, but it appears that further research is needed before we can say for sure exactly what might slow the progression of this common equine neurodegenerative disease.

Q: Should I seasonally alter the dose of Prascend in my PPID positive patients?

A: There is clear evidence that pituitary activity increases in the autumn. Some horses test normal throughout the year but positive (for PPID) in the autumn, other horses test routinely positive throughout the year with strong positives in the autumn.

Pergolide decreases pituitary activity, therefore it is logical to consider altering the dose of pergolide during the autumn seasonal rise.

Be aware that if a horse (with PPID) has its ACTH tested in August/September and a loss of endocrine control is identified and the dose of pergolide subsequently increased, by the time ACTH is checked again 30 to 60 days later, the seasonal rise is likely to have peaked and be almost over.

However, if it is established that a horse does lose endocrine control in the autumn, then the dose of pergolide could be increased the following July/August in preparation for the seasonal rise.

​It is a logical approach to increase pergolide for the seasonal rise; it needs further research, but many people have adopted this approach already

​Body condition scoring (BCS), or fat scoring, is a method of assessing the amount of fat a horse is carrying, and can help owners recognize whether their horse is over or under weight. It should be carried out regularly, ideally every 2 weeks, so that weight gain or loss can be acted upon appropriately.

There are two systems in use:

The 9 point system, developed by Dr Henneke. 6 parts of the body - neck, withers, shoulders, ribs, loins and tailhead - are given a score from 1 to 9, with a body condition score of 5 being considered ideal for leisure/riding horses, and a BCS over 7 indicating obesity.

​This video (below) by Dr Teresa Hollands - as shown in the October 2013 The Laminitis Revolution 2 webinar - shows how to body condition score your horse, using the modified 0-5 point scoring system. Horses that are too thin, too fat and just right are used to demonstrate how to assess BCS, including a typical underweight PPID horse and a typical overweight EMS/PPID pony.

The body should be divided into 3 sections: neck, middle and bottom, and each section scored separately by feeling for fat over the skeleton. 3 is the perfect score. Body condition scoring should be carried out ideally every 2 weeks on all horses, and the results recorded.

Neck - there shouldn't be any fat or crest above the nuchal ligament - there is no muscle above the nuchal ligament, anything felt here is fat, not top line. A large crest will score 4 or more, bulges and corregation in the crest will probably score 5.The shoulder blade should be well defined - if you run your hand down the side of the neck, it should come to a stop at the shoulder blade.

Middle - you should be able to feel the ribs, like feeling stair banisters through a velvet curtain, but hardly see them. If you can neither see nor feel the ribs, that scores 4 or more. If you place your hand over the backbone, it should form a nice curve - a triangle is too thin, flat is too fat.

Bottom - you should be able to feel just feel the top of the pelvis, the hip bone and the tail bone. If you can't see or feel these bones, that scores 4 or more.

Research has shown that if a horse is overweight, for the all fat that is visible or can be palpated under the skin, there is probably the same amount inside the horse that can't be seen, wrapped around the organs and killing the horse from the inside.

In summary, if you can feel AND see bones, the horse is too thin.If you can neither feel nor see bones, the horse is too fat.If you can feel but not see bones, the horse is just right.

​In this video from World Horse Welfare, a native pony is assessed and found to have a body condition score of 4.5/5, meaning he is on his way from fat to obese.

​In this video from Dodson & Horrell, two similar horses are body condition scored - the first has a body condition score of 3.5-4/5, the second has a perfect body condition score of 3/5.

In this video from The Blue Cross, use of a weight tape is demonstrated, and a pony is body condition scored and given a score of 4.

]]>Fri, 03 Jul 2015 17:38:17 GMThttp://www.thelaminitissite.org/articles/pituitary-pars-intermedia-dysfunctionPituitary Pars Intermedia Dysfunction, or PPID, is an endocrine disease that can affect any horse, pony or donkey, regardless of breed, sex or management. It’s a progressive, degenerative disease, so incidence increases with age and it generally has a slow insidious onset, making it difficult to detect and diagnose in the early stage. The excess hormones produced affect various body systems, and individual horses can show different symptoms, some of which can be serious, like laminitis. PPID used to be called Equine Cushing’s Disease, as there were thought to be similarities with Cushing’s Disease in humans and dogs, which involves a tumour that causes high levels of ACTH to be produced in the pars distalis of the pituitary gland, leading to high levels of cortisol, but no neurodegeneration. However, PPID in horses is different and is caused by neurodegeneration, affects the pars intermedia of the pituitary gland, and causes high levels of several hormones, but cortisol levels are often normal.

The pituitary gland lies below the hypothalamus at the bottom of the horse’s brain. It consists of three major hormone-releasing lobes: the pars distalis, the pars nervosa and the pars intermedia. All horses, whether they have PPID or not, react to stress by releasing ACTH from the pars distalis into the blood. This tells the adrenal glands to release cortisol, which plays a role in the “fight or flight” response. The high levels of cortisol in the blood “feed back” on the pars distalis, reducing ACTH production. In a normal horse, the pars intermedia plays a role in seasonal changes, metabolism and inflammation, producing a peptide called POMC, which is initially changed to ACTH, then around 98% of that ACTH is changed to alpha-MSH, beta-endorphin and CLIP before being released into the blood. This hormone production is slowed or stopped when neurons originating in the hypothalamus release dopamine (a neurotransmitter or chemical messenger) onto receptors on the pars intermedia. The pars intermedia is stimulated by the hormone TRH – this can be manipulated for diagnostic testing.

With PPID, the dopamine-producing neurons in the hypothalamus slowly degenerate, and with less dopamine to inhibit hormone production, the pars intermedia releases massively increased amounts of alpha-MSH, beta-endorphin, CLIP and also ACTH, which are thought to cause the clinical signs of PPID. The excess ACTH produced in horses with PPID may be less biologically active than normal, which may explain why horses with PPID often have normal cortisol levels, even when blood tests report high ACTH levels.As in any factory, increased production leads to expansion - the pars intermedia cells increase in number (hyperplasia) and size (hypertrophy), often leading to adenoma (benign tumour) formation, and causing the pars intermedia to increase in size (a normal pituitary gland weighs around 2 g, in a horse with advanced PPID it can weigh more than 10 g), which may cause compression of the other lobes of the pituitary gland.

What causes PPID?

The cause of PPID is still unknown, but research suggests that localised oxidative stress may contribute to dopaminergic neuron damage and cell death. Dr Dianne McFarlane found decreased activity of the antioxidant manganese superoxide dismutase in the pars intermedia in older horses, which could contribute to the risk of PPID developing with age, and she also found evidence of protein misfolding in the pars intermedia of horses with PPID, similar to that found in Parkinson’s disease. Inher presentation on the Pathophysiology of PPID at the 2011 Equine Endocrinology Summit, Dr McFarlane suggested that there may be several syndomes that lead to PPID,such as metabolic disorders like EMS, toxins in the environment, stress or genetic predisposition. This might explain why individual horses with PPID can have differing symptoms and hormone levels.

Diagnosis of PPID Diagnosis of PPID is based on clinical signs and history, backed up by above normal ACTH blood test results. Although incidence increases with age, horses as young as 6 or 7 have been diagnosed with PPID.

Percentage of horses aged 15+ showing symptoms suggestive of PPID. 21% were diagnosed as having PPID based on a resting ACTH result above the seasonally adjusted reference range.

Clinical signs The clinical signs seen vary between horses and with the stage of the disease, and are often mistaken for normal ageing. Experts often group clinical signs into early or advanced stage, but there is likely to be overlap. Symptoms are often worse during the autumn “seasonal rise”.

Abnormal sweating/thermoregulation – hyperhydrosis (increased sweating) or anhydrosis (lack of normal sweating). Sweating may be patchy and in unusual places.

Significant weight loss.

Polyuria/polydipsia (increased drinking and urination).

Abnormal haircoat – from a thicker than normal summer coat, long coarse hairs in the coat or patches of long hair to a long shaggy coat (hypertrichosis) that doesn’t shed at all.

Hyperglycaemia (above normal blood glucose concentrations).

Neurological symptoms such as ataxia, seizures and blindness.

It has been considered that hypertrichosis – the long coat that doesn’t shed – is diagnostic of PPID, but whilst it is highly suggestive, there can be other causes, such as severe malnutrition.

Scooby on arrival at Remus Horse Sanctuary showing hypertrichosis and muscle loss, and after being clipped and starting treatment for PPID.

It is currently thought that some but not all horses with PPID will also be at risk of laminitis – they have PPID and Equine Metabolic Syndrome (EMS), and are likely to have insulin dysregulation and abnormal fat deposits, e.g. cresty neck, filled supra-orbital hollows and fat around the tailhead, in addition to other symptoms of PPID. To identify these horses and assess laminitis risk, insulin dysregulation should be measured in all horses suspected of having PPID. Horses with PPID that have never had laminitis and that have normal insulin may not be at greater risk of developing laminitis than any other horse.

Although it isn’t yet known whether having EMS causes PPID, it seems that horses with EMS may be at greater risk of developing PPID as they get older, and therefore horses with EMS should be monitored and tested for PPID, and their diet, weight and exercise addressed with the aim of reversing EMS. Vets are also noticing that there appears to be a transitional period as horses with EMS develop PPID during which their insulin concentrations and therefore risk of laminitis increase.

Blood testsAs PPID is a progressive disease, blood tests are often negative in the early stages, but false positives are also seen when ACTH is released as part of the normal stress response. Hormone levels are affected by seasons and geographical location, are released in pulses so concentrations can change within minutes, and vary considerably between affected horses.

Resting ACTH concentration, which requires a single blood draw and can be done at any time of the day or year, as long as seasonally adjusted reference ranges are used (see Liphook Equine Hospital's weekly cutoff values for ACTH), and the horse is not stressed before or during the blood collection. Note that ACTH can be measured using different assays, with different reference ranges, therefore results from laboratories may not be comparable. Horses in the UK that have not been diagnosed with PPID may be eligible for a free ACTH test – see http://www.talkaboutlaminitis.co.uk/.

When resting ACTH results are borderline or negative despite a suspicion of PPID, the TRH stimulation of ACTH may be recommended. A resting ACTH blood sample is collected, then 1 mg of TRH is injected and a further ACTH blood sample collected 10 minutes later. Horses with PPID appear to produce more ACTH in response to an injection of TRH than normal horses. Currently this test cannot be used in the autumn, and more research is required to define normal reference ranges.

All horses suspected of having PPID should be tested for insulin dysregulation using either a resting insulin test, or if no clinical signs of insulin dysregulation are seen and/or if resting insulin test results are normal, an oral sugar test, to assess laminitis risk. The dexamethasone suppression test, once considered the gold standard for PPID testing, is no longer recommended as it may cause laminitis, requires two vet visits, cannot be used in the autumn, and may only detect advanced cases. Tests measuring cortisol are not diagnostic for PPID.

All horses have a “seasonal rise” in pars intermedia hormone production in the autumn, probably to help them prepare for the winter, which starts as days begin to get shorter and is considered significant from August to October. The increase is greater in horses with PPID, making this the best time to test ACTH, as long as seasonally adjusted reference ranges are used.

A diagnosis of PPID should only be made if there are clinical signs of PPID. There is no way of knowing whether the ACTH in a blood sample is from the pars intermedia and suggests PPID if abnormally high, or has been produced by the pars distalis as part of a normal stress response. “Stress” can be due to pain (e.g. laminitis), illness, excitement, exercise, travelling, use of a twitch, veterinary procedures e.g. dental work or “white coat phobia”. Some medicines may increase ACTH, e.g. clenbuterol (Ventipulmin) and some sedation durgs, and current advice (from Liphook Equine Hospital) is that ACTH should not be tested following sedation. Note also that freezing the blood sample before it has been separated by centrifuge can lead to falsely high ACTH results.

In the future, testing of other PPID hormones may be commercially available, which may make blood testing more accurate.

Treatment

PPID currently cannot be cured, but can be treated with daily oral administration of a dopamine agonist such as pergolide (licensed for horses as Prascend in many countries), which replaces the missing dopamine, signalling the pars intermedia to reduce hormone production, and thereby reducing the clinical signs of PPID. It isn’t currently known whether treatment with pergolide will prevent or slow the hyperplasia and hypertrophy associated with the excess hormone production of the pars intermedia, but in theory this seems possible.

In addition, research by Gille et al. (2002) found that pergolide protects dopamine-producing neurons under conditions of elevated oxidative stress, and Dr McFarlane has theorised that any antioxidant and neuroprotective properties of pergolide could be beneficial in slowing the progression of PPID, suggesting that early treatment with pergolide may be advisable.

The initial dose of Prascend recommended is 0.002 mg/kg bodyweight once a day, so 1 mg for a 500 kg horse, but the dose may depend on the stage of the PPID, the season and other factors, and it should be titrated to the lowest effective dose for each individual horse based on response to therapy, whether that is improvement in clinical signs and blood results or signs of intolerance. Many horses require an increased dose during the seasonal rise, with a subsequent reduction in dose around Christmas.

Some horses go off their food or become depressed when starting treatment with pergolide, but when introduced gradually, ideally starting with 0.25 mg and slowly increasing to the recommended dose, side effects are minimised. Giving pergolide at different times to bucket feeds has helped some horses overcome inappetence.Response to treatment is individual, but the EEG suggests that within 30 days of starting treatment an improvement in lethargy and depression, PU/PD and blood glucose concentrations should be seen, with improvements in haircoat abnormalities, improved topline and reduced incidences of laminitis and infections within a year. In The Laminitis Site’s experience, improvements are often noticed sooner than this, particularly when the PPID has not yet reached the advanced stage.

Blood should be tested 30 - 60 days after starting pergolide to assess response to treatment. PPID horses treated with pergolide and retested every 4 weeks showed significant reductions in resting ACTH levels, but TRH stimulation of ACTH results rose initially, suggesting resting ACTH may be more suitable for monitoring response to treatment.

It is suggested that horses with PPID have blood tests every 6 months, with one test during the seasonal rise (ideally August), to monitor the progression of the disease and their response to treatment.

Currently there is no research that supports the use of herbal, homeopathic or other non-medical treatments for PPID. Some owners report improvements in depression and coat shedding with Vitex agnus castus, but research by Jill Beech et al. (2002) found no improvement in hormone levels and that clinical signs sometimes worsened when PPID horses were treated with Vitex agnus castus.

Management is also very important and should be optimized. Excess hair should be clipped and rugs used to help regulate the horse’s body temperature. The diet should contain above minimum levels of quality protein, minerals, vitamins and essential fatty acids, with energy levels appropriate for the horse’s lifestyle, and sugar and starch amounts kept low if the horse has insulin dysregulation. In theory feeds high in antioxidants could help to slow the neurodegenerative process that causes PPID, but there is currently no evidence for this. Attention should be paid to dental care, foot care, worming and vaccinations, and infections should be treated without delay.

ConclusionWhilst there is still a lot to learn about PPID, recent advances in our knowledge have enabled horses to be diagnosed and start treatment much earlier in the disease process, with the result that many horses with PPID are living quality lives well into old age.

This article was originally published in The Arabian Magazine July 2015 and has been updated since publication.

]]>Sat, 20 Jun 2015 00:30:10 GMThttp://www.thelaminitissite.org/articles/equine-metabolic-syndrome-and-insulin-dysregulationRecognising and treating Equine Metabolic Syndrome (EMS) is essential to improve insulin sensitivity and reduce the risk of laminitis. Experts also now suspect that horses with EMS may be at greater risk of developing PPID as they get older. EMS is not a disease, it is a cluster of factors that indicate that a horse is at greater risk of developing endocrinopathic laminitis. It is preventable and reversible with correct management.

Often seen in “easy keeper” breeds including native ponies, Arabians, Morgans and Iberians, a horse with EMS will usually have:

1. General obesity or regional adiposity (a cresty neck, filled supraorbital hollows, fat behind the shoulders and around the tailhead, swelling around the sheath/mammory glands);

3. A predisposition to or history of laminitis - signs of chronic laminitis such as hoof rings wider at the heels, a less-than-tight white line and a change of angle in the hoof wall may be seen in the feet, and x-rays may show rotation and remodelling of the pedal bone.

ObesityObesity develops when horses have too much food and too little exercise. As the horse becomes obese and fat cells become full, the insulin signaling pathway is disrupted, causing insulin resistance. Fat cells release pro-inflammatory chemicals that cause systemic inflammation, and hormones including leptin, a “stop eating” hormone released when the horse has excess energy stored. High levels of leptin cause the target cells to become less receptive, or resistant, to the message to stop eating, so the horse continues to eat and put on weight. Obesity may also affect liver function resulting in reduced insulin clearance and consequent hyperinsulinaemia.Research has suggested that weight gain has a greater impact on insulin sensitivity in certain breeds, with Arabians becoming insulin resistant when fed excess energy, but Thoroughbreds showing no decrease in insulin sensitivity with weight gain.

Measurements to help identify obesity should be carried out regularly (e.g. every 2 weeks):

1. Cresty neck score from 0 to 5, with scores of 3 or greater often being seen in horses with EMS. A cresty neck score of 3 is described as “Crest enlarged and thickened, so fat is deposited more heavily in middle of the neck than towards poll and withers, giving a mounded appearance. Crest fills cupped hand and begins losing side-to-side flexibility.”

Owners of horses and ponies in Great Britain can register for the Care About Laminitis study and monitor their horse's weight online.

Genetics Some breeds appear to be more predisposed to EMS than others and there is likely to be a genetic tendency, but developing EMS may depend on certain environmental factors being present, or multiple genes being involved. For example, scurry ponies in active competition tend to have low insulin concentrations, but insulin levels rise when they are not in work, suggesting that exercise helps to prevent them developing EMS.

Breeds adapted to survival when feed is scarce, e.g. cold winters, summer droughts, may be particularly likely to become obese and develop insulin resistance when they have plentiful food all year round.Native ponies naturally gain weight during the summer when food is abundant and lose weight during the winter, and without these seasonal changes in body condition and insulin sensitivity, horses may become increasingly obese and insulin resistant.

Insulin

In 2007 it was first discovered that giving healthy horses high levels of insulin caused them to develop laminitis (Asplin et al.). It is hyperinsulinaemia, i.e. above normal levels of insulin, not insulin resistance, that causes endocrinopathic laminitis, but they are often linked, hence the term “insulin dysregulation” is now used to cover both hyperinsulinaemia and insulin resistance.

When a healthy horse eats sugar or starch, blood glucose levels rise and the pancreas releases insulin, which enables glucose to enter insulin sensitive cells, such as muscle.

When an insulin resistant horse eats sugar or starch, blood glucose levels rise and the pancreas releases insulin, but the insulin sensitive cells don’t respond to normal amounts of insulin and glucose doesn’t enter the cells efficiently. The pancreas compensates by releasing more insulin, which enables glucose to enter the cells and keeps blood glucose levels reasonably normal, but results in increased blood insulin levels, or hyperinsulinaemia.

This is illustrated in research by Katie Borer et al. published in 2012. Ponies with no history of laminitis (normal) and ponies with a history of laminitis (laminitic) were fed ad lib soaked Timothy hay and a daily feed of 14% sugar/starch chaff, to which 1 g/kg bodyweight of glucose, fructose and inulin, a type of fructan, were added. The previously laminitic (therefore assumed to have EMS) ponies had a much greater insulin response to glucose than the normal ponies, but their blood glucose levels showed less difference. Note that chaff plus fructan had no greater effect on insulin or glucose than chaff alone.

Diagnosis of insulin dysregulation

1. Resting insulin - a single blood sample is tested, either after the horse has fasted for at least six hours or after eating hay. “Testing horses in the fed state allows for better assessment of insulin dysregulation” (Frank and Tadros 2013), but results may be harder to interpret if sugar/starch levels of the hay are not known. Results above 20 mIU/ml are often considered diagnostic of hyperinsulinaemia, but the reference range is specific to the testing laboratory. When the horse is fasted, this test has a false negative rate of around 70%, therefore a normal result does not rule out EMS, and a dynamic test (Oral Sugar Test) should follow.

2. Oral sugar test (OST) – the horse is fasted for at least 6 hours then fed 0.15 ml/kg bodyweight Karo Light corn syrup and blood sampled at 60 and 90 minutes and tested for insulin and glucose. Insulin <45 mIU/ml is considered normal and >60 mIU/ml is considered diagnostic of insulin dysregulation. Recently (2017) it has been suggested that a higher dose Oral Sugar Test can be carried out without the horse having to be fasted beforehand, using 4.5 ml/kg bodyweight Karo Light corn syrup. See Karo Light Corn Syrup test for assessment of insulin dysregulation - Liphook Equine Hospital.This test measures the horse’s response to sugar in the diet at the level of the digestive system, pancreas and insulin sensitive tissue.

Current tests are not reliable and horses strongly suspected of having insulin dysregulation often test negative, so diagnosis of EMS should be based on history and clinical signs as well as blood test results. Pain and stress, as well as feed, may increase insulin and glucose levels.

Managing horses with EMSDiet, weight loss if necessary and exercise are key to preventing and treating EMS.

Diet/weight loss

The total combined sugar and starch in the diet should be no more than 10% to keep insulin levels low, and if weight loss is required, energy fed will need to be less than energy expended. The severity of the horse’s hyperinsulinaemia will dictate how strict the sugar/starch restriction needs to be.

Some experts consider non-structural carbohydrates (NSC) to be important – NSC is sugars or ethanol soluble carbohydrates (ESC), fructans and starch, with ESC plus fructans forming water soluble carbohydrates (WSC). Others consider only ESC and starch to be important, as these directly affect insulin, but not fructans.

Low sugar/starch, high fibre forage e.g. grass hay should form the basis of the diet, ideally analysed for ESC and starch content (Equi-Analytical in the USA analyse ESC, WSC and starch), with protein, minerals, vitamins and essential fatty acids supplemented to meet minimum requirements.

Vitamin E, copper, zinc, selenium and sodium are typically deficient in hay. Hay can be soaked in water to reduce sugars, although the amount of sugar loss is variable and may depend on the amount of water used, the temperature of the water, how fibrous the hay is and other factors. A popular myth is that old hay is better for laminitics – according to Katy Watts of www.safergrass.org, the only nutrients correctly made and stored hay will lose over time are vitamins, not sugars.

Low energy feeds should be selected to maximise intake without oversupplying calories. Looking at the analysis of feeds rather than the description is important, e.g. some "high fibre" cubes contain almost 20% combined sugar and starch and would not be suitable for most EMS horses, and feeds claiming to be approved or suitable for laminitics can contain over 14% combined sugar and starch.

Grass will often provide too much energy and be too high in sugar/starch for an EMS/overweight horse. Horses with insulin dysregulation that need to gain weight can be fed increased amounts of hay and/or higher energy low sugar/starch feeds such as umolassed sugar beet (beet pulp).

Weight loss is induced by restricting calories eaten and by increasing exercise if the feet are stable. A common suggestion is to feed a horse 1.5% of its ideal, or current, bodyweight (with the diet based on hay with added minerals as described above). If weight loss isn’t seen, this amount may need to be reduced, or ideally a lower energy forage sourced. Feed intake should not go below 1.2% of the horse’s bodyweight without veterinary supervision. Severe calorie restriction can worsen insulin resistance, risk hyperlipaemia and cause stereotypical behaviour.

GrassAccess to unrestricted grass commonly triggers laminitis in EMS horses, as sugars increase insulin levels and increased energy intake promotes weight gain. Access to grass should be restricted until insulin sensitivity has returned to normal, with horses turned out in a dry lot or dirt paddock if the feet are stable to encourage exercise. Many horses that have had EMS can return to pasture once weight has been lost and insulin sensitivity has returned to normal, but may need to have access to grass restricted during high risk times, such as during rapid spring growth or when grass is stressed and cannot grow due to cold weather or drought. Factors that affect sugars in the grass include:Sunlight - photosynthesis and sugar production increase with sunlight intensity, so sugar levels will be higher on sunny days and lower on cloudy, overcast and rainy days. Grass growing in direct sunlight will have more sugar than grass growing in the shade.Time of day – sugar levels peak around late afternoon on a sunny day, then decrease with respiration once the sun sets, so sugars are likely to be lowest in the early morning.Temperature – night temperatures below 5’C cause sugars to accumulate in the grass, and laminitic horses should avoid grazing during periods of sunny days and cold nights, until warmer nights or overcast weather returns.

Stress – grass needs water and nutrients to grow, and drought conditions or poor soil fertility can lead to increased sugar levels.

Grass species – improved species designed for cattle such as rye grass may have higher energy/sugar levels.

Strategies for limiting grazing include short turnout periods (less than 1 hour) or grazing in hand, turnout in a small area, use of a grazing muzzle and putting horses on a track system. Note that when access to grass is restricted, studies have shown that ponies can learn to eat grass quickly, eating almost half of their daily feed requirement in 3 hours of grazing (Longland et al. 2011).

Exercise

Regular physical exercise is likely to improve insulin sensitivity and help promote weight loss, and is recommended for EMS horses as long as the feet are stable. The ACVIM consensus statement suggests at least 2-3 sessions of 20-30 minutes of riding or lunging per week, gradually increasing in intensity and duration. Other recommendations for obese horses free of laminitis include riding or lunging 4 to 7 days a week with at least 30 minutes of trot and canter, plus warm up and cool down.See ExerciseMovement - good or bad?

Medication

The ACVIM consensus statement states “Most horses and ponies with EMS can be effectively managed by controlling the horse’s diet, instituting an exercise program, and limiting or eliminating access to pasture.”

Metformin is sometimes prescribed for horses that cannot exercise due to laminitis, at the dose of 30 mg/kg bodyweight twice a day. Giving this dose of Metformin before a glucose feed led to reduced glucose and insulin levels compared to controls, but the paper concluded that the potential benefits of giving Metformin to horses on a low NSC diet may be questionable (Rendle et al. 2013).

Supplements

Whilst various supplements such as magnesium, chromium and cinnamon have been suggested for the management of horses with EMS, currently there is insufficient scientific evidence to support the use of any of these supplements, and where research has been carried out, no or little benefit has been found. See There are no magic potions!

Is EMS reversible? In theory, yes, EMS is both preventable and reversible. EMS is not a disease, but a collection of factors that increase the risk of endocrinopathic laminitis. Remove these factors (being overweight, having regional fat deposits, having abnormally high insulin levels), and technically the horse no longer has EMS – although some horses with a stronger genetic tendency may always need more careful management than others. The reversal of obesity is likely to have the greatest influence on insulin sensitivity, so make weight loss a priority in overweight horses.

This overweight pony was diagnosed with EMS and laminitis. With careful management he lost his excess weight and fat pads and his insulin levels returned to normal – it can be done! Photo credit: Kat.

TTeam practitioner Danielle Dibbens has worked with The Laminitis Site on several laminitis rehabilitations, and has made a video showing how to carry out several TTouches suitable for horses recovering from laminitis.

Danielle emphasises that bodywork is complementary to veterinary care and that the cause of the laminitis should be identified and removed/treated, and the feet supported and realigned.

She begins by running her hands all over the horse and becoming aware of warm/cool, hard or bumpy areas, watching for feedback from the horse, feeling for textures, tone and temperature, and notes that the back, quarters and hamstrings are often tight in horses that have had laminitis. This is followed by:

Zebra Zigzag TTouch - can be used all over the body, may help to relieve muscular tension and reconnect the body when the horse's posture has changed following laminitis.

The pressures used are very light. These techniques can be used on any horse or pony and on other animals, and can be practised on friends and family to check and perfect your technique.

Include pauses to allow the horse to process information, and remember to breathe and smile when working with your horse.

Be aware of feedback from the horse, such as eye blinking, eye size, breathing rate, ear and head position, stepping away from or into the handler or lifting a leg. Be aware of the horse's comfort zones and areas that the horse may be protecting, and use approach and retreat to slowly increase access to protected areas.

Use EVA gym mats to support the feet if necessary - see EVA foam pads.

Disclaimer: The information, suggestions and links (hereafter referred to as “information”) contained in this video are provided for information purposes only and should not be relied upon nor replace professional veterinary advice. Information is non-veterinary, is based as far as possible on current research, does not constitute advice or diagnosis, and should be discussed with all relevant vets and hoofcare or other professionals. No responsibility is taken for the accuracy or suitability of information contained in this video, and no liability accepted for damages of any kind arising from use, reference to or reliance on any information contained in this video. It is your responsibility to take appropriate care of your own safety when working with horses. If you suspect your horse has laminitis or is ill, please consult your vet.

The philosophy of The Laminitis Site is “identify and remove/treat the cause, and support and realign the feet”. Thanks to recent research we are now much better at establishing and treating the cause to prevent further laminitis, but what about feet damaged by laminitis – can rotation and/or sinking (also called distal descent) be corrected?

Yes, absolutely. In many cases the hoof capsule can be realigned with the pedal bone, sinking distance may reduce, and the horse can return to its pre-laminitis level of soundness.

describing how a realigning trim that minimized hoof wall loading, sole protection with boots and pads, and movement, returned 14 out of 14 horses with endocrinopathic laminitis and rotation as severe as 29 degrees to their pre-laminitis level of soundness.

Take correctly marked x-rays Rehabilitation from laminitis starts with correctly marked lateromedial x-rays to assess the damage and to guide trimming. Any horse that has had clinical laminitis should have x-rays taken. Ponies in particular can have significant damage in their feet without appearing to be lame, and x-rays should be taken if external signs of chronic laminitis such as hoof rings wider at the heels than the toe, a stretched or deep white line or change of angle in the hoof wall are seen, so that rotation can be identified and corrected.

A change of angle in the hoof wall at the toe (red), high heels making a shallow hairline to ground angle (blue) and divergent hoof rings (yellow) suggest chronic laminitis in this pony. X-rays confirmed dorsal and palmar rotation and remodelling of the pedal bone.

Casareño, 6 months into his rehabilitation, has a straight hoof wall at the toe (red), a good hairline angle (blue), and one hoof ring (yellow), presumed to be linked to the single corticosteroid treatment that appeared to trigger laminitis. X-rays confirmed that the hoof wall was parallel to the pedal bone, and that his rehabilitation following laminitis was progressing well.

Case study: Sorrel, a Connemara pony with EMS and later diagnosed with PPID, had had laminitis on and off for 7 years and never had x-rays. Photos of her feet suggested that her heels were too high, the walls were flared with toe cracks, the frogs were not weight bearing and a deep black groove between wall and sole suggested white line separation.

X-rays showed significant rotation in both front feet, with a dorsal angle of rotation (red) of 20 degrees (her toes were too long and there was a significant laminar wedge) and palmar rotation (green) of 21 degrees (her heels were too high). A change in angle between the short pastern and pedal bone indicated bony rotation (purple), and she had little sole depth (blue). Assuming the hairline marker was correctly placed, she did not have significant sinking/distal descent (yellow).A vet suggested 8 months of specialist farrier work, shoes and box rest, but with a correct realigning trim and boots and pads she was soon able to have grass free turnout and in-hand exercise, and eight months after her realigning trim she was back in ridden work.

A lot of information can be obtained from clear well-marked x-rays:

Marking the hairline and wall at the toe allows calculation of the amount of sinking (technically referred to as the coronary band:extensor process distance or CE) – yellow, the dorsal angle of rotation – red, and the difference in dorsal horn and lamellar tissue thickness at the top and bottom of the pedal bone (hoof:lamellar zone) – pink.

A clear ground line enables the palmar angle – green, and sole depth – blue, to be calculated.

Marking the apex of the frog provides an important reference for trimming, and helps to determine whether the apex of the frog is true or has grown forwards.

An x-ray may also indicate areas of gas or fluid – orange (this horse was developing a sub-solar abscess), whether there has been remodelling of the pedal bone, and whether rotation is capsular and/or bony.

Compare this to an unmarked x-ray of a foot with similar rotation. Whilst the bones are well defined, without a hairline marker it is impossible to assess sinking, and without a hoof wall marker the dorsal angle of rotation and hoof:lamellar zone would be estimates. Without a clear ground line the palmar angle and sole depth can only be guessed at, and there is no way of telling the position of the frog apex. All this x-ray really tells us is that the horse has rotation, a significant gas pocket and so far no bone remodelling. Both x-rays are digital and cost much the same, but the x-ray above with the external markers provides much more valuable information, particularly for the hoof care professional.

The realigning trim If x-rays show rotation, a realigning trim should be carried out as soon as possible – while the foot is not correctly aligned, the horse is likely to be in pain, and the foot at risk of further damage. Dr Eleanor Kellon, in her online Cushing’s and Insulin Resistance course, states “ I firmly believe if more horses were trimmed correctly and aggressively from the start of their laminitis, we would see far fewer problems with chronic pain and eventual hoof deformity”.

In Care and Rehabilitation of the Equine Foot, Pete Ramey says “at the first signs of laminitis, restore P3 to a more natural ground plane, relieve pressure on the walls and pad the sole with foam rubber – vertical sinking and destructive pressure to the solar corium can be prevented”.

The principles of the trim are the same for every horse – the hoof should hug the bone, and the footprint should be normal. This means the hoof wall should return to being parallel to the dorsal surface of the pedal bone, and the solar surface of the pedal bone should return to making an angle of around 3-8 degrees with the ground (3-5 degrees may be more suitable following rotation, to minimize pressure on the solar corium beneath the tip of the pedal bone). Rehabilitation is not just about trimming - encouraging hoof to grow where needed can be just as important as removing hoof material.

The white hoof capsule of the rotated foot with long toe, inadequate sole depth and high heels returns to the red bone-hugging hoof capsule following realigning trimming.

1. trimming the hoof walls level with the sole plane and bevelling the outer wall at the toe and through the quarters to minimise weight bearing by the hoof walls – the hoof wall at the toe was trimmed out of contact with the ground. Dr Taylor suggests that whilst the deep digital flexor tendon does exert a rotational force on the pedal bone, it does not result in added stress to the laminae if the hoof wall at the toe is trimmed so that it is not weight bearing.

2. reducing the palmar angle by lowering the heels to just above the live sole plane, but without removing more than 10 mm in any one trim. The heels were lowered by rasping a heel plane approximately 2 to 3 degrees away from the solar plane of the pedal bone, and by floating the rasp above the front of the foot to preserve and develop sole depth.

3. not rasping hoof wall flare until two thirds of the hoof wall was new growth.

Laminitis causes the laminae to stretch and weaken. In theory, bevelling the hoof wall (purple line) to remove it from ground contact and therefore weight bearing, would decrease strain on the laminar attachments by removing the mechanical force of the horse’s weight (white arrow) opposing the hoof wall (yellow arrow), thereby minimizing or preventing further rotation or sinking. Following the realigning trim (purple toe bevel, pink heel plane) and with sole protection from boots and pads, the horse’s weight would be born by the sole, frog, heels and bars (blue arrows).

Floating the rasp – to lower the heels and reduce the palmar angle, but preserve and develop sole depth in the front of the foot, the rasp should be “floated”, ideally staying 15 mm above the bottom of the collateral grooves at all times, in effect putting a bevel on the heels. This is likely to leave the ground surface of the foot in two planes while the sole develops in thin soled horses, but using thick soft pads inside boots and/or deep conforming bedding allows for this.

Hoofcare professionals must “see” the internal structures and trim accordingly.

Above left: A typical realigning trim might involve:

Reducing the palmar angle by lowering the heels in 3 close-together trims as suggested by the pink lines (and dictated by the live sole plane) to create a heel plane parallel to the 3-4 degree palmar angle indicated by the green line.

Reducing the dorsal angle of rotation by bringing breakover back to or just in front of the black line drawn down the dorsal surface of the pedal bone to the ground, and allowing for adequate sole depth. With the toe bevelled to remove it from weight bearing, as suggested by the purple line, new tightly connected wall will grow down from the coronary band parallel to the pedal bone. Laminar separation doesn’t just occur at the toe – the outer wall should be bevelled to or past both quarters.

Developing sole depth by ensuring that the area marked orange is protected, by “floating” the rasp 15 mm above the bottom of the collateral grooves.

The actual areas of hoof that might be trimmed are marked yellow, the areas that would not be trimmed are marked orange.

Above right: After 3 trims the hoof print would be almost normal, and the hoof should look like this once the sole has developed and the new hoof wall grown down from the coronary band.

Case study: Nutmeg’s owner first contacted The Laminitis Site just hours before Nutmeg was due to be put to sleep because of rotation following probably years of chronic laminitis due to EMS and PPID. X-rays showed > 20 degrees of dorsal and palmar rotation, she was in a lot of pain and vets considered that her feet had been damaged beyond repair. Information on www.thelaminitissite.org helped Nutmeg’s farrier to carry out a realigning trim, and she started to improve immediately, being comfortable without pain relief for the first time in seven years. With boots and pads fitted she was soon going for in-hand walks and being turned out in a mud paddock.

Following trim guidelines marked on x-rays taken towards the end of Nutmeg’s rehabilitation, together with short trimming intervals, led to improvements in the dorsal and palmar angles.

A year after Nutmeg should have been put to sleep, her owner reported that she was doing well, was comfortable without pain relief and enjoying her daily walks. She said “it has been a big learning curve this year but Nutmeg is proof that it can be done, and getting her feet right was mainly due to having x-rays done and getting the trims just right to enable Nutmeg to have a good, comfortable quality of life.”

Protect the soles To protect and minimize pressure on the weight bearing soles, hoof boots with foam rubber pads were the first choice for Dr Taylor’s rehabilitation cases, with an air space under the rim of the pedal bone where soles were very thin (i.e. less than 7 mm), and pea gravel once horses had developed reasonable sole depth and were comfortable. Barefoot turnout was not allowed until horses had at least 12 mm of sole depth and were comfortable on the terrain without hoof protection. The sole can support the pedal bone through laminitis rehabilitation as long as it is well protected during weight bearing and as long as solar pressure is eliminated during hoof flight – this may be critical to maintain solar blood flow and prevent solar corium injury.Introduce movement Under Dr Taylor’s rehabilitation protocol, once the hooves had been bevelled to minimize weight bearing by the hoof wall, a palmar angle of less than 10 degrees had been established, the feet were well protected by soft pads inside hoof boots and the horse was comfortably landing heel first, turnout in a grass-free paddock and in-hand exercise were started. Exercise appeared to increase comfort, and was built gradually as long as the horse continued to land heel first and showed no discomfort.

After following Dr Taylor’s rehabilitation protocol, all the horses returned to their pre-laminitis level of soundness, despite all starting with dorsal rotation > 5 degrees and 6 horses having dorsal rotation > 11 degrees. Significant improvements were seen in dorsal rotation, palmar rotation, H:L zone thickness and sole depth, and there was a slight reduction in sinking. Increased heel volume was also noted.

Case study: Casareño, a 16 year old Andalusian, developed laminitis with rotation in all four feet in May after having a corticosteroid injection for a suspected pastern joint sprain. Shoes and heel wedges were fitted. Casareño got worse. His owner contacted The Laminitis Site and a realigning trim was suggested, but his vet declared this could be “a disaster”, saying that although the shoes could come off, the long toes and high heels should not be corrected until more sole depth had developed. The rotation worsened, and his owner feared Casareño could be heading towards euthanasia.

In August the first realigning trim was carried out following TLS guidelines, and x-rays showed reductions in both dorsal and palmar angles. Casareño was finally comfortable without pain relief. Despite the complications of a sub-solar abscess on the right fore and thrush in his frogs, often seen when heels have been left high, with regular trims guided by x-rays, by October Casareño had returned to in-hand exercise wearing boots with thick soft pads.

Casareño's owner recently said "everyone is amazed by Casareño's recovery. The situation seemed desperate at first, now my vet and farrier are referring Casareño's case to other clients."

Note that in the October x-ray the drawing pin marking the frog apex is further forwards in relation to the tip of the pedal bone. Frog and sole material often stretches forward following laminitis, and hoof care professionals must be certain that landmarks used to guide the trim are reliable. Using the x-ray, the approximate position of the true frog apex was projected onto the foot (brown line), and Casareño’s farrier was able to find the true apex and trim the frog accordingly.

“Too many horses fail to recover from laminitis due to incorrect trimming”– ECIR Group Inc and Dr Eleanor Kellon

Horses can and should recover from rotation and sinking following endocrinopathic laminitis, and the earlier problems are identified and corrected, the better the chance of a successful outcome. Horses have recovered from solar penetration and full sloughing of their hoof capsules, and can be made comfortable even with considerable pedal bone loss, once a correct realigning trim and foot protection are in place.

Every spring rapidly growing grass will trigger endocrine laminitis in many horses, ponies and donkeys, which may result in euthanasia if correct treatment and foot care are not received. Around 90% of all laminitis cases are now thought to have an endocrine cause - that is, they are due to “insulin dysregulation” - and are often associated with a diet high in sugar or starch (the other 10% of cases being inflammatory or supporting limb laminitis). Horses with endocrine laminitis will have Equine Metabolic Syndrome (EMS) with or without PPID (Pituitary Pars Intermedia Dysfunction), formerly known as equine Cushing’s disease.

What is laminitis?In a healthy horse the hoof wall wraps around the pedal (coffin) bone and is connected to it by laminae (also called lamellae) - interlocking cells often compared to velcro. The abnormally high levels of insulin seen with endocrine laminitis appear to cause the laminae to stretch and weaken, often leading to the hoof capsule and bone moving away from each other – rotating and/or sinking - under the horse's weight. This can damage tissue, blood supply and nerves, causing pain, and eventually cell death, bone loss and sepsis if the damage is left uncorrected. Laminitis is described as chronic once rotation and/or sinking have occurred.

Hoof rings wider at the heels than at the toe suggest chronic laminitis (thanks to Laura for photo use)

How is laminitis recognised?

Symptoms of laminitis vary considerably, and range from the horse appearing to be sound but having signs of chronic laminitis in the feet (e.g. hoof rings wider at the heels, a stretched white line and radiographic changes), through the horse being “footy” or short-strided on hard ground, unwilling to turn or trot, shifting weight from foot to foot and having a bounding digital pulse, to lying down most of the time with an increased heart and respiration rate. Laminitis can quickly progress from mild to severe and should always be taken seriously.More..

How is laminitis treated?The cause must be identified and removed/treated, and the feet must be supported and fully realigned. With correct treatment, even significant damage to the feet can often be repaired and the horse returned to health.

Laminitis should always be considered an emergency – call the vet, and farrier/trimmer.

Ensure the feet are well supported with full solar surface conforming padding.

EVA floor mats cut to size and secured with duct tape provide good support for laminitic feet

Confine the horse on deep conforming bedding to limit movement (pad the feet before moving the horse to the area of confinement, and keep movement to a minimum, e.g. by using a low-loading trailer).

Remove the horse from grass and feed a high fibre <10% sugar/starch diet based on analysed or soaked hay, plus minerals, vitamins, protein and essential fatty acids to meet minimum requirements. Never starve a horse with laminitis because of the risk of inducing hyperlipaemia – feed at least 1.2% of the horse’s bodyweight per day. More..

Pain relief such as Bute or Danilon may be prescribed to reduce the pain but is unlikely to treat the laminitis – it is now recognised that there is little inflammation involved in endocrine laminitis. If pain relief is still required after a week, it’s likely either the cause of the laminitis hasn’t been correctly identified and removed/treated, and/or the feet haven’t been correctly supported and realigned, and the case should be reassessed.

X-rays should be taken immediately to identify dorsal and palmar rotation, sinking, sole depth and pockets of gas/fluid.

The feet should be trimmed as soon as possible to correct any dorsal and palmar rotation, to relieve pressure on the outer walls and to maximise weightbearing on the less painful structures at the back of the foot.

Once pain is controlled, blood should be tested for insulin, ACTH and glucose to aid the diagnosis of EMS and PPID.

Equine Metabolic Syndrome EMS is not a disease but a cluster of factors that increase the risk of laminitis. Often seen in “easy keeper” breeds including native ponies, Arabians and Iberians, a horse with EMS will usually have:

obesity and/or regional fat deposits (e.g. a cresty neck, filled supraorbital hollows, fat behind the shoulders, around the tailhead or around the sheath/udder);

insulin dysregulation - hyperinsulinaemia or insulin resistance; and

a predisposition to or history of laminitis.

This mare with EMS has a large solid neck crest with “sausage-like” fat deposits, a dip in front of the withers, and filled supraorbital hollows. A lack of shoulder definition, gullet along her spine and inability to feel her ribs easily indicate that she is very overweight - see Rosie

Hyperinsulinaemia (above normal insulin levels) is known to cause laminitis

This overweight pony was diagnosed with laminitis and EMS, aged 6. After a year of careful dieting, he achieved his ideal weight, his fat pads disappeared and his insulin returned to normal (thanks to Kat for photo use)

Diagnosis is based on blood tests showing above normal insulin levels after fasting or eating low sugar hay, or an oral sugar test, plus symptoms and history. However, tests are often falsely negative so a normal result does not rule out EMS. Glucose may be tested but is usually normal.

Treatment is weight loss if necessary, a low sugar/starch diet that provides all essential nutrients, and exercise when the horse is able. The human antidiabetes drug Metformin is sometimes prescribed when a horse has high insulin levels and cannot exercise due to laminitis, but drug treatment should not be a substitute for correct diet.

Note that the use of corticosteroid drugs increases insulin levels, and carries a high risk of causing laminitis in susceptible horses.

Pituitary Pars Intermedia DysfunctionPPID is a progressive disease that starts when dopamine-producing neurons in the brain die, possibly due to oxidative damage, causing the pars intermedia in the pituitary gland to release excessive amounts of several hormones (alpha-MSH, beta-endorphin, ACTH and CLIP), and eventually leading to enlargement of the gland.

Reduced dopamine from the hypothalamus causes an increase in hormone production from the pars intermedia, and consequent increase in size of this area of the pituitary gland

Clinical signs vary between horses and the stage of the disease, and include muscle loss, a pot belly, lethargy, recurrent infections, increased worm burdens, infertility, weight loss and abnormal sweating, and horses with PPID and EMS may have laminitis, insulin dysregulation, abnormal fat pads and excess drinking/urination. The long curly coat that doesn’t shed is a sign of advanced PPID, but early signs include long hair on the legs, face and neck, and late or patchy shedding. Symptoms are often worse in the autumn.

Early PPID can be hard to diagnose with the tests currently available – blood tests are often negative and signs of PPID overlap with normal ageing. Diagnosis is based on above normal ACTH (adrenocorticotropic hormone) plus clinical signs and history. Testing ACTH between August and October may give the best results, using seasonal reference ranges, and the TRH (thyrotropin releasing hormone) stimulation of ACTH may be used outside of these months if resting ACTH results are equivocal. Some experts believe that not all horses with PPID are at increased risk of laminitis, and insulin should be tested to identify those that are.

PPID is treated with daily pergolide (now licensed for horses in many countries as Prascend) to replace the missing dopamine, plus optimized management, with attention to providing a diet that provides all essential nutrients, clipping and rugging if necessary, good dental and foot care and targeted parasite control.

Horses with EMS appear to be at greater risk of developing PPID as they get older, and may have a greater risk of laminitis as they transition from EMS to PPID.

How can laminitis be prevented? The good news is that many cases of endocrine laminitis can be prevented with careful management and simple daily checks for at-risk horses:

Keep horses at their correct weight and body condition score – carry out a hands-on body condition score assessment and check weight using a weight tape, weight calculation or weigh bridge at least twice a month. Allow horses to lose weight naturally over the winter months if they are likely to gain a little weight in the spring. If weight loss is required, aim for the horse to lose no more than 0.5 – 1% of bodyweight per week, do not feed less than 1.2% of bodyweight unless under veterinary supervision, and ensure essential nutrients are provided by the diet.

Restrict or prevent grazing when grass is growing fast (increased quantity) or is stressed by drought or cold sunny weather (increased sugar). Consider using a grazing muzzle, track system and/or strip grazing to limit grass consumption and encourage movement. Seewww.safergrass.orgfor information about sugar levels in grass.

A grazing muzzle combined with track system allows horses with insulin dysregulation to socialise and exercise (thanks to Fiona for photo use) - see Sorrel's case study

Ensure horses are regularly exercised as long as their feet are correctly aligned and stable. If exercise is reduced, consider reducing the energy content of feed – many cases of laminitis follow a reduction in exercise due to lameness, rider illness/holiday or bad weather.

Keep feet perfectly balanced and supported, and check regularly for any signs of chronic laminitis – if signs are seen, have x-rays taken and ensure feet are fully realigned as soon as possible.

Be vigilant for clinical signs of EMS and PPID, and arrange blood tests if suspicious – the aim is to diagnose and treat these conditions before laminitis occurs.

Daily checks that can help early identification of laminitis include:

Walking the horse on hard ground – there should be no decrease in stride length, no suggestion that the horse is “footy” or “pottery”, and the horse shouldn’t seek out softer ground.

Turning the horse in a tight circle to the left and right – the turns should be fluid with no reluctance.

Checking the digital pulse in the pastern or fetlock – it shouldn’t be more bounding than normal.

Monitoring fat pads – any increase in size or firmness of neck crest, supraorbital filling, fat around the tailhead and udder or sheath swelling could indicate increased laminitis risk.

Supraorbital hollows – normal on the left, filled on the right (thanks to Liz for photo use)

Testing insulin levels forms part of the diagnosis of Equine Metabolic Syndrome (EMS), and gives information about insulin dysregulation and laminitis risk. All horses suspected of having PPID should also have insulin tested to assess their laminitis risk.

There are currently no perfect tests for diagnosing EMS or insulin dysregulation. The pros and cons of the tests currently available "in the field" are discussed below.

Resting insulin tests

This is the easiest test to carry out and involves taking a single sample of blood to measure the amount of insulin in the horse's blood at that moment in time. It can be either:

1. Fasting resting insulin - the horse is fasted for at least 6 hours before the blood is collected.This test has a high false negative rate (around 2/3 of horses with insulin dysregulation have a normal fasting insulin result), so a normal test result does not rule out EMS, and a dynamic or non-fasted resting test should follow a normal fasting insulin test if a horse is suspected of having insulin dysregulation. If a horse gets stressed from having food withheld - this may be a particular problem on a yard where other horses are being fed and the horse being tested isn't - this could falsely increase the result.

Interpretation:Results above the laboratory cut-off are diagnostic of hyperinsulinaemia.Whilst a cut off of 20 mIU/l is often used, reference ranges for insulin are laboratory specific - the reference range given by the testing laboratory should be used. Note that different assays, e.g. RIA v CIA, may produce different results meaning that results cannot be compared.

Reference ranges for insulin may be breed specific, therefore a cut-off of 20 µIU/ml may not be appropriate for all breeds.

TLS comment: due to the high number of false negatives, this test is probably only worth doing if a horse obviously has EMS/insulin dysregulation (e.g. history of laminitis, overweight, fat pads), but the test is diagnostic, accepted by vets, and good for monitoring progress when positive.

2. Non-fasting resting insulin - the horse eats hay or grass but no bucket feed in the 6 hours before the blood is collected.Allowing the horse access to food before the resting insulin test measures the horse's insulin response to its normal diet. But if the amount of sugar in the diet isn't known, this adds uncertainty to the test and makes a borderline result more difficult to interpret. This was the test recommended by vets/researchers until a few years ago, generally using a cut off of 30 uIU/ml (rather than the 20 uIU/ml cut off used for the fasting test). Presumably because hay can have differing sugar levels, vets/researchers have decided this test isn't as accurate as the fasting test. However, it's unlikely hay is going to push a "normal" horse over a cut-off of 30 uIU/ml, or even 20 uIU/ml.The ECIR group recommends that low sugar/soaked hay is in front of the horse at all times before the test - DDT Diagnosis of PPID and IR.TLS comment: there seem to be less false negatives with this test and it gives an accurate reflection of the horse's actual day to day insulin levels, but there may be a grey area around the cut-off due to unknown sugar levels in the hay/grass. With no fasting and no abnormally raised insulin levels involved, it is safe and is probably the test a horse would choose!

Dynamic insulin tests

This measures the horse's insulin response after eating glucose/sugar - a high result suggests insulin dysregulation, therefore it should be a good test for determining which horses are at higher risk of getting laminitis. However dynamic tests can also give false negative results - Dianne McFarlane suggested that half the horses she tested that she pretty much knew had EMS tested negative - Is it PPID or is it EMS?

If a baseline (resting) sample is taken before the glucose is fed, the increase in insulin as a result of eating the glucose can be measured.If insulin is only measured after the horse has eaten the glucose, it isn't possible to know how much the insulin increased as a result of eating the glucose - the horse could have had an above normal insulin concentration even after fasting for several hours.

A dynamic insulin test can be either:

3. Oral Sugar Test (OST) - this uses 0.15 ml/kg bodyweight Karo Light corn syrup, which gives around 75 g sugar to a 500 kg horse, which isn't totally unlike a horse eating grass - say a 500 kg horse eats 2.5% of his bodyweight in 12% ESC/starch grass (fructans don't appear to increase insulin, grass doesn't tend to have more than around 12% simple sugars, after that simple sugars are turned into fructans), that would be 1500 g sugar, over 16 hours grazing, so 94 g sugar/hr of grazing. So 75 g in a few minutes is still likely to be far more than a horse can eat naturally, but it's a lot better than the in-feed glucose test. All research done to validate this test (and the in-feed glucose test) has been done with the horse fasting for at least 6 hours beforehand, so for these dynamic tests the horse should be fasted for accurate interpretation.

4. In-feed Glucose ChallengeThe in-feed glucose challenge uses a large amount of glucose (either 1 g or 0.5 g per kg bodyweight, so 500 or 250 g for a 500 kg horse), an amount that a horse could not eat in its natural diet. One problem with this is that glucose enters the blood through glucose transporters, which can become saturated. When a horse is used to having a lot of sugar in its diet, it will increase the number of glucose transporters (this has been proven by feeding increasing amounts of starch). But when a horse is usually on a low sugar diet and is suddenly fed a huge amount of glucose, a large amount of this may be unable to be absorbed in the small intestine and will be carried through to the hind gut. So the number of glucose transporters will have an effect on the insulin result. And the test could potentially cause diarrhoea, gas and colic - we have had reports of diarrhoea following the test using 1g/kg bw glucose.

As can be seen from the paragraph above, this amount of glucose is FAR more than a horse can possibly eat naturally. So although this test has been used in research to distinguish horses with EMS from horses without EMS, all it really tells you is how much insulin your horse will produce if given a massive amount of sugar that it couldn't possibly get hold of. Sadly we now have loads of horses being treated with Metformin following this test, when they would almost certainly test normal on a hay-fed resting insulin test - i.e. their day to day life is controlling their insulin.

The in-feed glucose challenge measures how much insulin a horse secretes (and then cannot clear) when it eats a large amount of glucose quickly. It doesn't measure how that horse might respond to its normal diet.

Horses with EMS can have very high insulin results with the in-feed glucose test, over 800 uIU/ml. We know that this insulin level causes laminitic changes in the feet when kept at that level for 6 hours. Whilst the insulin level caused by the test will peak and then fall, the damage caused by exposure to these high levels of insulin for less than 6 hours hasn't been looked at.

TLS suggestions for diagnostic testing:

If a horse has had laminitis or has any clinical signs of EMS, such as being overweight, having a cresty neck or fat pads, start with a resting insulin test - fasting or low sugar hay is a decision for the owner. If this test is negative, then an oral sugar test will give an idea of that horse's insulin response to sugar. However, a positive OST is not a reason to start treatment with Metformin, it indicates that diet, weight control and exercise should be improved.

If a horse has never had laminitis and has no obvious signs of EMS, but seems the type of horse that might be susceptible, then going straight to the OST seems justified, as a resting insulin would be quite likely to come back negative, and the OST shouldn't raise insulin significantly if the normal diet isn't doing so.

For PPID horses with no signs of EMS and that have never had laminitis, either start with a resting insulin or go straight for the OST. All horses with PPID should have insulin tested. If there really is no suspicion of EMS then going straight to the OST is probably justified. But if there's the slightest suspicion of EMS, it's probably best to start with a resting insulin.

Conclusion:Resting insulin - best place to start for horses that have had laminitis or are pretty likely to have EMS;Oral sugar test - best place to start for horses that have never had laminitis and have no obvious signs of EMS.TLS does not recommend the in-feed glucose challenge.

Monitoring

Insulin is tested to diagnose EMS/insulin dysregulation, to assess laminitis risk and potentially to quantify how significant any laminitis risk is likely to be. Following initial diagnosis, insulin should continue to be tested to monitor improvements in insulin regulation, until the horse's insulin levels remain normal on his usual diet.

The factors that cause/contribute to insulin dysregulation/hyperinsulinaemia/insulin resistance can and must be managed or treated so that insulin levels return to normal, or as close to normal as possible. Remember that EMS is not a disease, it is a cluster of risk factors that increase the risk of laminitis, and these risk factors can be reduced, often to the point where the horse is at no greater risk of laminitis than any other horse, as long as it is managed carefully.

This might mean:Overweight horses lose weight until they reach their correct weight.Levels of sugar and starch in the diet are kept low - generally total NSC or ESC plus starch in the diet should be below 10%; some horses may require diets with lower levels of sugar and starch.Exercise is introduced/increased if the horse's feet are stable and correctly aligned and supported.PPID is assessed as a cause of hyperinsulinaemia and treated if present.Corticosteroid use is avoided or discontinued (under veterinary supervision).Some horses appear to have a stronger genetic disposition to insulin dysregulation than others - they are likely to need stricter management of the above factors.

To monitor improvement, it is often suggested that the test that was used for diagnosis be repeated under the same conditions. However, what we probably most need to know is whether the horse has above normal levels of insulin every day when eating its usual diet. If an initial fasting resting insulin was positive, continue to test this under the same test conditions until a normal result is seen. Once fasting resting insulin is normal (or if a non-fasting resting test was the initial test used), next time test resting insulin with the horse eating his normal hay. When that is normal, if you want to return the horse to grazing, test resting insulin with the horse eating a restricted amount of his normal grass. If the grass causes an above normal insulin result, then you know you probably need to restrict grass further or eliminate grazing completely. If you get a normal insulin result after restricted grazing, you can probably continue to allow access to grass, monitoring closely for signs of laminitis/EMS and testing insulin as often as you can. There's no science behind this, but it seems logical.

Frequently Asked QuestionsQ. What is insulin resistance?A. When a normal horse eats, glucose is absorbed into the blood stream and insulin is released to enable that glucose to enter insulin sensitive tissue – blood levels of both glucose and insulin rise after a meal and then drop back down.

When a horse with insulin resistance eats, glucose is absorbed into the blood stream and insulin is released, but the insulin sensitive tissue (primarily muscle) does not respond normally to that insulin, which prevents glucose in the blood from entering the tissue normally. The pancreas "compensates" by producing more insulin to ensure that glucose does enter the tissue - blood levels of insulin increase and take longer to drop back down (compensatory hyperinsulinaemia). Q. What mechanisms can cause high levels of insulin?

A. Insulin can be increased because of:

1. hyperinsulinaemia without insulin resistance - e.g. hormones produced in excess when a horse has PPID may cause excess insulin to be produced, regardless of diet - it is possible that CLIP could be responsible for this - it has been shown to raise insulin in pigs. Chronic hyperinsulinaemia (and hyperglycaemia) are likely to lead to tissue insulin resistance.

2. insulin resistance at the level of the tissue (muscle), leading to compensatory hyperinsulinaemia (see above).

3. reduced clearance of insulin by the liver.

If a horse has greater than normal absorption of glucose or greater than normal release of insulin from the pancreas, over time the horse can develop insulin resistance at the level of the tissue - a dynamic oral test will pick up dysfunction at every level. However, if you only use dynamic and not resting tests, you don't know whether the insulin result after feeding sugar/glucose is due purely to the sugar/glucose, or whether it would have been above normal without the sugar/glucose.

A. A reliable positive fasting resting insulin result should be sufficient for a diagnosis of EMS/insulin dysregulation, together with clinical signs and history. There is no need to carry out a glucose challenge test as well, particularly as a horse with an above normal resting insulin may have a very high insulin response to glucose. Management changes should be made (reduced sugar/starch diet, weight loss, increased exercise if appropriate) and PPID eliminated as a possible cause of the above normal insulin, and resting insulin retested under the same conditions until a normal result is achieved. At this point you might consider carrying out the oral sugar test, to see whether the horse still has an abnormal insulin response to sugar, or testing resting insulin when the horse is eating his normal diet, as above.